For convenience we can divide physicians into two camps: those who follow the IDSA and those who follow ILADS. This is an over-simplification. Many physicians fall in between. I am seeing more infectious disease physicians cross over into the chronic Lyme side of things. Many other physicians are becoming more interested in treating Lyme as a chronic disease and treating it as such. The paradigm has broadened for many of us; chronic Lyme has evolved into chronic tick borne disease. Many patients do not improve or recover, at least not fully, unless other co-infections are treated as well. The treatment of co-infections exposes Lyme aware physicians to increased criticisms by IDSA leaning physicians because the presence of these entities is frequently more difficult to demonstrate than Lyme--Borrelia burdorferi.
Readers must be reminded that in the main, laboratory evidence suggesting the presence of Babesia tells the physician only one thing: the patient has been exposed to Babesia. Here I am referring to serological antibody tests. Other, more convincing tests, for the non-believers, include a blood smear which shows the organisms or a FISH test offered by IgeneX. These tests are not particularly sensitive missing most cases. Serologically, we can test for two strains of Babesia through commercial labs: B. microti and B. duncani. There are numerous other strains of Babesia for which no simple test exists. Clongen lab can perform a Babesia "species" PCR test which is very specific but not all that sensitive. It screens for the presence of Babesia DNA for about 15 species of Babesia.
In routine lab panels described elsewhere, anybodies directed against B. microti and B. duncani or WA1 are routinely obtained. It is always nice to have one's clinical suspicions mirrored in a laboratory test. But like most things Lyme: the diagnosis of Babesiosis is a clinical one.
Many clinical signs and symptoms have been ascribed to Babesiosis. In my practice the primary symptom is sweating. Patients have night sweats, sweats after a hot shower, day sweats or chills and flu like symptoms which recur cyclically. A secondary feature is muscle pains in preference to joint pain.
Another helpful test is the evaluation of a wet mount slide. Many patients show a crescent shaped organism which resembles Toxoplasmosis. I do not believe this organism is Toxo: many patients with the organism have negative serology (antibodies) directed against Toxo. I will explain why I mention this finding in connection with Babesiosis in a moment.
The standard treatment for Babesiosis has been Mepron, usually combined with Zithromax.
Mepron is a yellow liquid which is unpleasant tasting and very expensive. It contains a single ingredient: Atovaquone. Malarone, on the other hand, contains two anti-parasite ingredients: Atovaquone and Proguanil. Malarone is a less expensive, convenient tablet.
Malarone seems to address this crescent shaped parasite whereas Mepron does not. It is my suspicion that this other, yet unknown parasite, is responsible for much muscle pain, including that associated with fibromyalgia syndromes.
Even though the dose of Atovaquone in Malarone is only 1/3 of that present in Mepron, I have found it is effective for Babesia symptoms. My experience has informed me that it is the length of therapy, not the dose of Atovaquone which helps ameliorate Babesia related symptoms and presumably infection. Anti-Babesia or parasite therapy can be augmented by adding the herbal medicine, Artemsin, usually 200mg twice daily.
So yes, there are more positive serologies for B. duncani than B. microti here on the east coast which contrasts with the views of local health officials, still, the diagnosis of this syndrome is made strictly on clinical grounds. There exists a subset of patients with antibodies to Babesia who never exhibit symptoms of this infection. Most of these patients improve even though this specific co-infection has not been treated. Presumably, in these cases, the infection was mild and eliminated by a well functioning immune system. Even so, the presence of these antibodies can be used to substantiate the diagnosis of chronic Lyme in patients who are Lyme seronegative: where there is smoke there is usually fire.
A basic rule of thumb which has served me well for over 25 years of medical practice still holds: treat the patient, not the labs.
Another comment: Zithromax is not very is not very effective against Lyme disease; its cousin macrolide Biaxin is. Biaxin is frequently avoided when antibiotics are combined because of its it "sloppy" tendency to cause adverse drug to drug interactions: it doesn't play well with others.
Biaxin may reduce blood levels of Atovaquone by 40%. Still, in patients where the treatment of Lyme is imperative along with the treatment of Babesia, this combination has still been effective in many patients.
Another, quite effective drug can be mixed with Malarone for Lyme disease: Cleocin. But this drug carries its own unique risks, especially C. diff colitis, the nemesis of physicians treating chronic Lyme and related disorders. As always the need for probiotics can not be stressed enough. I prefer the combination of Sacchromyces with an Acidophilus mix.
Tuesday, July 14, 2009
Wednesday, July 8, 2009
Ambien and a bump to the head with surprising consequences
A 42 year old female was in good health until she took an Ambien one night to help with some insomnia. Apparently she got up during sleep (sleep walking), went into the kitchen, and began to cook a meal. She then proceeded to fall down and bang her head. She presented to my office with a headache, some dizziness and severe pain and swelling in her lower extremities. Her calf muscles were extremely swollen and tender. I was concerned that she might have a subdural hematoma ( a clot in the skull) or rhabdomyolysis, a condition of muscle breakdown after injury which can lead to kidney failure. I sent her to the ER for a work up. The results were negative.
She came back in a day later. Her calf muscles were increasingly tight, swollen and painful. I was worried about a DVT (a blood clot). I sent her for a duplex (ultrasound) study to exclude this. It was negative. The pain was increasing in intensity. Narcotics, at a fairly high dose were needed to control the pain. The Percocet was not working; she returned with tears streaming down her face. She did not have myositis--inflammation of the muscles because the muscle enzyme CPK or CK was normal. Did she has some sort of myopathy? I ran some blood tests for an autoimmune disease. Oddly, her rheumatoid factor was elevated at 285. New symptoms appeared: there was now a tremor of her arms. I started a tapering dose of steroids. It was of no help.
She came back in a day later. Her calf muscles were increasingly tight, swollen and painful. I was worried about a DVT (a blood clot). I sent her for a duplex (ultrasound) study to exclude this. It was negative. The pain was increasing in intensity. Narcotics, at a fairly high dose were needed to control the pain. The Percocet was not working; she returned with tears streaming down her face. She did not have myositis--inflammation of the muscles because the muscle enzyme CPK or CK was normal. Did she has some sort of myopathy? I ran some blood tests for an autoimmune disease. Oddly, her rheumatoid factor was elevated at 285. New symptoms appeared: there was now a tremor of her arms. I started a tapering dose of steroids. It was of no help.
A neurological exam was performed. Deep tendon reflexes were absent across the board. Pin prick sensation was decreased in a stocking/glove pattern affecting all limbs. Vibratory sensation was minimal in the feet. A tick borne disease panel was ordered.
The results: Lyme ELISA IgM 0.91--equivocal range, Lyme WB 41 IgM and IgG bands, Babesia WA1 antibody elevated 1:256, C6 peptide 0.2, CD57 63. Did she in fact have tick borne illness? Had trauma activated a latent tick borne infection leading to an autoimmune syndrome with progressive symptoms in a previously well individual? That was my thinking.
And her symptoms were progressive--rapidly. She developed uncontrolled rhythmic seizure like jerking of her arms. This was associated with uncontrolled vocalizations typical of Tourettes syndrome. The pain and muscle swelling continued to be severe and difficult to manage. She developed night sweats. None of these symptoms existed prior to her traumatic injury.
Treatment for Lyme and Babesia with typical antimicrobials over a 2 month period has been successful. The neuro symptoms--the seizures and Tourettes resolved. The pain and swelling has lessened. She is now returning to work half time, a feat which would have been unimaginable a few weeks ago.
This is the clinical vingette.
These are my thoughts--conjectures.
There are a large number of patients who harbor Lyme (Bb) and its associated co-infections without clinical illness. These parasitic entities are contained by the host and its immune system.
The healthy state can be quite tenuous. Many things can unleash the ticking bomb: intercurrent infection, stress or even physical trauma.
The percent of individuals in endemic areas who are assymptomatic carriers of TBD may be much higher than suspected, given my suspicion that the vast majority of infected individuals exhibit no symptoms of disease.
A positive Lyme ELISA test should not be discounted when the second tier--the Western Blot is negative. Any positive result for Lyme: ELISA, Western Blot or C6 peptide should be considered as potential evidence of the disease.
Positive tests for Babesia WA1 or Babesia duncani have become extremely common, much more so than B. microti. There has to date been no acknowledgement of this change in distribution of this parasite from the west coast to the east coast by health departments.
There are better sleeping medications than Ambien.
And her symptoms were progressive--rapidly. She developed uncontrolled rhythmic seizure like jerking of her arms. This was associated with uncontrolled vocalizations typical of Tourettes syndrome. The pain and muscle swelling continued to be severe and difficult to manage. She developed night sweats. None of these symptoms existed prior to her traumatic injury.
Treatment for Lyme and Babesia with typical antimicrobials over a 2 month period has been successful. The neuro symptoms--the seizures and Tourettes resolved. The pain and swelling has lessened. She is now returning to work half time, a feat which would have been unimaginable a few weeks ago.
This is the clinical vingette.
These are my thoughts--conjectures.
There are a large number of patients who harbor Lyme (Bb) and its associated co-infections without clinical illness. These parasitic entities are contained by the host and its immune system.
The healthy state can be quite tenuous. Many things can unleash the ticking bomb: intercurrent infection, stress or even physical trauma.
The percent of individuals in endemic areas who are assymptomatic carriers of TBD may be much higher than suspected, given my suspicion that the vast majority of infected individuals exhibit no symptoms of disease.
A positive Lyme ELISA test should not be discounted when the second tier--the Western Blot is negative. Any positive result for Lyme: ELISA, Western Blot or C6 peptide should be considered as potential evidence of the disease.
Positive tests for Babesia WA1 or Babesia duncani have become extremely common, much more so than B. microti. There has to date been no acknowledgement of this change in distribution of this parasite from the west coast to the east coast by health departments.
There are better sleeping medications than Ambien.
Friday, June 19, 2009
Lyme disease and female hysteria
I offer this piece after reading only the abstract of a recently published article. There may be inaccuracies because I have not read the entire piece. Feel free to post corrections.
A syllogism is a form of logical thinking which I learned about in college. Syllogisms are frequently twisted into false logic causing spurious or misleading conclusions. To say( 1) more women have Lyme disease(which is vague) then (2)more women also have depression(which is also vague) THEREFORE women who have Lyme disease likely have depression- is like saying: fire hydrants are red: you are red: therefore you are likely a fire hydrant. This is the sort of logic evinced in a recent article published by prominent anti-Lyme IDSA figures in the Journal of Women's Health. I can understand why women take umbrage with these remarks.
Not only is the logic false, but the implications are insulting to many health care professionals and professional health care organizations. If "Chronic Lyme disease" is a vaguely defined term that has been applied to patients with prolonged subjective symptoms..." The same cannot be said for fibromyalgia, chronic fatigue or depression.
Fibromyalgia is not vague. It is a syndrome which has been clearly described by the American Association of Rheumatology. It is defined by very specific symptoms combined with very specific physical findings. Chronic fatigue syndrome is not vague. It has been very clearly defined. This definition can be viewed in CDC published literature. Depression is certainly not vague. The psychiatric community has meticulously defined this disorder, and its subtypes, in a book called the DMS4.
There are clear cultural differences between men and women. Men are infrequent users of the health care system. Men are less likely to complain of symptoms. Culturally men are taught to be stoic, to not complain and ignore symptoms until they are very advanced.
Their are indeed biological differences between men and women as well. Women are twice as like to suffer with autoimmune diseases as men. Most physicians who treat chronic Lyme disease are well aware of the strong autoimmune component of Lyme disease. Women also live longer than men and are less likely to succumb to severe infectious illnesses. These differences are real.
Are diseases like depression really more common amongst women? We know that women are more likely to seek professional help for depression. MEN ARE FOUR TIMES MORE LIKELY TO SUCCESSFULLY COMMIT SUICIDE. Which gender is more depressed? Men are more likely to suffer with alcoholism, drug addiction and commit acts of violence. These are well known surrogates of depression and other mental illnesses.
The word "hysteria" is derived from an ancient Greek medical concept. It was a female disease related to a disturbance of the uterus. Hysteria has become synonymous with the terms "psychosomatic" and "psychogenic." Sadly, many physicians today are still influenced by this ancient, unwarranted prejudice.
One might conclude that the authors have lumped together these so called female predominant disorders because the underlying beliefs of the authors, like many others in the medical community, is that these "new age" illness are a phony-psychosomatic- manifestation of hysteria- as described by the ancient Greeks.
Why conclude that so called chronic Lyme patients have been misdiagnosed and really have these other syndromes? What evidence is there to back up this conclusion? Perhaps it is the other way around. Typically, chronic Lyme patients do not neatly fit into the syndromes of fibromyalgia or chronic fatigue syndrome. Unfortunately may cynical physicians, who fail to accept the reality of these illness, have used these clinical disorders as a "waste basket" for Lyme patients when in fact no clear diagnosis has been established--at least according to their paradigm.
This sort of thinking seems dismissive and anachronistic with regard to the suffering of so many chronic Lyme sufferers. And as stated at the outset, the logical argument marshaled here is questionable at the very least.
One has to question the motives of the authors: Are they trying to promote a scientific understanding of a disease or are they publishing pabulum in an effort to promote their pre-existing, crumbling paradigm?
I think its time for a change. Don't you?
A syllogism is a form of logical thinking which I learned about in college. Syllogisms are frequently twisted into false logic causing spurious or misleading conclusions. To say( 1) more women have Lyme disease(which is vague) then (2)more women also have depression(which is also vague) THEREFORE women who have Lyme disease likely have depression- is like saying: fire hydrants are red: you are red: therefore you are likely a fire hydrant. This is the sort of logic evinced in a recent article published by prominent anti-Lyme IDSA figures in the Journal of Women's Health. I can understand why women take umbrage with these remarks.
Not only is the logic false, but the implications are insulting to many health care professionals and professional health care organizations. If "Chronic Lyme disease" is a vaguely defined term that has been applied to patients with prolonged subjective symptoms..." The same cannot be said for fibromyalgia, chronic fatigue or depression.
Fibromyalgia is not vague. It is a syndrome which has been clearly described by the American Association of Rheumatology. It is defined by very specific symptoms combined with very specific physical findings. Chronic fatigue syndrome is not vague. It has been very clearly defined. This definition can be viewed in CDC published literature. Depression is certainly not vague. The psychiatric community has meticulously defined this disorder, and its subtypes, in a book called the DMS4.
There are clear cultural differences between men and women. Men are infrequent users of the health care system. Men are less likely to complain of symptoms. Culturally men are taught to be stoic, to not complain and ignore symptoms until they are very advanced.
Their are indeed biological differences between men and women as well. Women are twice as like to suffer with autoimmune diseases as men. Most physicians who treat chronic Lyme disease are well aware of the strong autoimmune component of Lyme disease. Women also live longer than men and are less likely to succumb to severe infectious illnesses. These differences are real.
Are diseases like depression really more common amongst women? We know that women are more likely to seek professional help for depression. MEN ARE FOUR TIMES MORE LIKELY TO SUCCESSFULLY COMMIT SUICIDE. Which gender is more depressed? Men are more likely to suffer with alcoholism, drug addiction and commit acts of violence. These are well known surrogates of depression and other mental illnesses.
The word "hysteria" is derived from an ancient Greek medical concept. It was a female disease related to a disturbance of the uterus. Hysteria has become synonymous with the terms "psychosomatic" and "psychogenic." Sadly, many physicians today are still influenced by this ancient, unwarranted prejudice.
One might conclude that the authors have lumped together these so called female predominant disorders because the underlying beliefs of the authors, like many others in the medical community, is that these "new age" illness are a phony-psychosomatic- manifestation of hysteria- as described by the ancient Greeks.
Why conclude that so called chronic Lyme patients have been misdiagnosed and really have these other syndromes? What evidence is there to back up this conclusion? Perhaps it is the other way around. Typically, chronic Lyme patients do not neatly fit into the syndromes of fibromyalgia or chronic fatigue syndrome. Unfortunately may cynical physicians, who fail to accept the reality of these illness, have used these clinical disorders as a "waste basket" for Lyme patients when in fact no clear diagnosis has been established--at least according to their paradigm.
This sort of thinking seems dismissive and anachronistic with regard to the suffering of so many chronic Lyme sufferers. And as stated at the outset, the logical argument marshaled here is questionable at the very least.
One has to question the motives of the authors: Are they trying to promote a scientific understanding of a disease or are they publishing pabulum in an effort to promote their pre-existing, crumbling paradigm?
I think its time for a change. Don't you?
Monday, June 15, 2009
The accidental patient
I just saw a 32 year old female. This is the patient that I dread to see. She saw my associate for a routine physical. My associate does not treat Lyme disease. The patient complained of severe brain fog, memory loss, inattention and confusion. These alarming symptoms had been increasing over a period of several years. She even told my associate that she felt like she was developing Alzheimer's disease--at age 32. My associate ordered a few lab tests; she threw in a Lyme WB. The results: IgG 41 and 39 bands present. This meets the IgeneX criteria for a positive Lyme test. According to IgeneX the presence of these two bands indicates Lyme exposure with specificity of 96%. Of course IgeneX is looking at their own assay; there is no real basis for transposing this data to WBs obtained elsewhere, even though his may seem logical.The patient researched her symptoms on the Internet. Lyme disease frequently popped up on her browser. She is confused. Does she have Lyme disease? If so, how is it treated. Internet sources inform her that treatment ranges from 28 days to lifelong. How is a medical consumer to make sense of this and other contradiction? Throw more in the mix: She is trying to get pregnant, now what? Can Lyme be passed to the fetus? She has read this on line. On the other hand, aren't antibiotics dangerous to a developing fetus and just dangerous in general.
My exam showed peripheral neuropathy: nothing else concrete.
Cognitive problems are difficult to prove. For the most part the patient's subjective report of symptoms is all you really have to go on. Neuro-psychological testing can be ordered but these tests are nearly impossible to interpret without a before and after. By the time patients present we only have the "after." The tests are expensive, time consuming and rarely covered by insurance companies. What then?
A brain MRI and brain SPECT scan are good starting point. They may be normal or abnormal.
If the brain MRI shows white matter changes a neurologist might to chalk it up to migraine , early MS or vasculitis. A rheumatologist will likely concur: vasculitis. A psychiatrist might suggest depression.
Further Lyme WBs may be positive or negative. Co-infection testing may be positive or negative. From the perspective of other physicians I have found that little credence is given to these results even when they are positive.
This young woman with very troubling symptoms showed up on my schedule for 15 minutes to review "lab results." If not for the 39 band on a WB she probably would never have seen me.
It became my job to introduce her to a medical parallel universe, within the allotted time.
Being an "LLMD," if that is what I am- can sometimes feel like a curse. Ignorance is bliss. But I became a doctor to help people- that is who I am- that is what I do.
How do this tell this young woman that she is lucky she came to see me on this day?- it sounds arrogant, even to me. She may see countless other physicians who will conclude that she definitely does not have Lyme disease. As an "erstwhile" neurologists friend once quipped: "Why is it that you know something that no one else knows?" Why indeed.
I am amongst the very few that believe in chronic Lyme or for that matter the existence of neuroborreliosis it seems. I get no support from local colleagues or local medical institutions held in high esteem who believe my views are incorrect and misguided. Furthermore, they point to the dangers of long term antibiotic therapy for a non-existent illness.
I have but 15 minutes to inform and instruct her. All I can do is order the tests outlined below and give her a lot of reading material. I can ask her to watch Under Our Skin--which my patients tell me is now difficult to find. I direct her to "Cure Unknown" and the ILADS website.
My blog is not a good starting point. It is generally only helpful for those already steeped in the Lyme debacle.
I do not know if she will follow through with any of my recommendations. Lyme patient's with cognitive deficits have trouble reading and processing to start with.
And then there is the problem with family members. They dismiss the diagnosis of Lyme disease and frequently ridicule it. It doesn't exist. They disparage the treating doctor(s) and offer no validation of the patient's suffering or pain. This may lead to depression and feelings of alienation and hopelessness. The high fees charged by many physicians further reduces their credibility in the minds of many.
No this is not the patient I want to see. Not today. Perhaps selfishly I would rather see the patient who has already seen 40 other doctors, those who know more about the nuances of Lyme than I do. If I charged high fees the uninitiated would be weeded out: life would be so much easier.
Treating such patients(the one described here) is a risky business. It is not insurance companies who have "turned me in," contrary to public belief. No, it is my colleagues, members of the IDSA, who have been anxious to report me to the Medical Board.
The anger which I once had is gone. It is pointless and emotionally draining. As the smoke has cleared I am overcome with a new found sense of humility. After all- who I am really- a lone voice shouting into an empty wind only to hear the echo of my own voice.
I put myself into the patient's shoes. How can this one doctor have special knowledge about my illness? It admittedly does not meet the sniff test. She may ultimately see an assortment of specialist who may politely or not so politely tell her that I am a quack- or just wrong at best. Although it is not Lyme disease, no diagnosis will be found. Perhaps years later she will come back with a progressive, mustisystem illness- perhaps with an infected child. Or maybe, after looking into the matter she will decide to return for me to treat her. Time will tell. I cannot control the decisions of others. I can only control my own decisions.
I have no confidence that the IDSA "review" of its guidelines will bring us any closer to the truth.
The public debate in DC is set to occur this July. ILADS is armed with great speakers and a plethora of facts and published scientific studies. But ultimately the IDSA will be passing judgment on itself. How can the accused party fairly judge itself? This runs contrary to human nature.
The light of truth will eventually shine on this national disgrace known as Lyme disease. How long this will take? Nobody knows. We do our best and sail on through the still stormy seas.
I love being a doctor, I always have. Still--some days I wish I were a fisherman, sailing into challenging whimsical ,unpredictable seas-seeking elusive tuna or other prizes.
Perhaps this is what I do after all.
My exam showed peripheral neuropathy: nothing else concrete.
Cognitive problems are difficult to prove. For the most part the patient's subjective report of symptoms is all you really have to go on. Neuro-psychological testing can be ordered but these tests are nearly impossible to interpret without a before and after. By the time patients present we only have the "after." The tests are expensive, time consuming and rarely covered by insurance companies. What then?
A brain MRI and brain SPECT scan are good starting point. They may be normal or abnormal.
If the brain MRI shows white matter changes a neurologist might to chalk it up to migraine , early MS or vasculitis. A rheumatologist will likely concur: vasculitis. A psychiatrist might suggest depression.
Further Lyme WBs may be positive or negative. Co-infection testing may be positive or negative. From the perspective of other physicians I have found that little credence is given to these results even when they are positive.
This young woman with very troubling symptoms showed up on my schedule for 15 minutes to review "lab results." If not for the 39 band on a WB she probably would never have seen me.
It became my job to introduce her to a medical parallel universe, within the allotted time.
Being an "LLMD," if that is what I am- can sometimes feel like a curse. Ignorance is bliss. But I became a doctor to help people- that is who I am- that is what I do.
How do this tell this young woman that she is lucky she came to see me on this day?- it sounds arrogant, even to me. She may see countless other physicians who will conclude that she definitely does not have Lyme disease. As an "erstwhile" neurologists friend once quipped: "Why is it that you know something that no one else knows?" Why indeed.
I am amongst the very few that believe in chronic Lyme or for that matter the existence of neuroborreliosis it seems. I get no support from local colleagues or local medical institutions held in high esteem who believe my views are incorrect and misguided. Furthermore, they point to the dangers of long term antibiotic therapy for a non-existent illness.
I have but 15 minutes to inform and instruct her. All I can do is order the tests outlined below and give her a lot of reading material. I can ask her to watch Under Our Skin--which my patients tell me is now difficult to find. I direct her to "Cure Unknown" and the ILADS website.
My blog is not a good starting point. It is generally only helpful for those already steeped in the Lyme debacle.
I do not know if she will follow through with any of my recommendations. Lyme patient's with cognitive deficits have trouble reading and processing to start with.
And then there is the problem with family members. They dismiss the diagnosis of Lyme disease and frequently ridicule it. It doesn't exist. They disparage the treating doctor(s) and offer no validation of the patient's suffering or pain. This may lead to depression and feelings of alienation and hopelessness. The high fees charged by many physicians further reduces their credibility in the minds of many.
No this is not the patient I want to see. Not today. Perhaps selfishly I would rather see the patient who has already seen 40 other doctors, those who know more about the nuances of Lyme than I do. If I charged high fees the uninitiated would be weeded out: life would be so much easier.
Treating such patients(the one described here) is a risky business. It is not insurance companies who have "turned me in," contrary to public belief. No, it is my colleagues, members of the IDSA, who have been anxious to report me to the Medical Board.
The anger which I once had is gone. It is pointless and emotionally draining. As the smoke has cleared I am overcome with a new found sense of humility. After all- who I am really- a lone voice shouting into an empty wind only to hear the echo of my own voice.
I put myself into the patient's shoes. How can this one doctor have special knowledge about my illness? It admittedly does not meet the sniff test. She may ultimately see an assortment of specialist who may politely or not so politely tell her that I am a quack- or just wrong at best. Although it is not Lyme disease, no diagnosis will be found. Perhaps years later she will come back with a progressive, mustisystem illness- perhaps with an infected child. Or maybe, after looking into the matter she will decide to return for me to treat her. Time will tell. I cannot control the decisions of others. I can only control my own decisions.
I have no confidence that the IDSA "review" of its guidelines will bring us any closer to the truth.
The public debate in DC is set to occur this July. ILADS is armed with great speakers and a plethora of facts and published scientific studies. But ultimately the IDSA will be passing judgment on itself. How can the accused party fairly judge itself? This runs contrary to human nature.
The light of truth will eventually shine on this national disgrace known as Lyme disease. How long this will take? Nobody knows. We do our best and sail on through the still stormy seas.
I love being a doctor, I always have. Still--some days I wish I were a fisherman, sailing into challenging whimsical ,unpredictable seas-seeking elusive tuna or other prizes.
Perhaps this is what I do after all.
My basic panel of tests ordered for the evaluation of suspected tick borne disease
The diagnosis of Lyme disease is made on clinical grounds. Nonetheless, these are routine test- I suppose standard tests, ordered for many of my patients suspected of having tick borne illness-
CBC
Chem panel-CMP
Sed rate
CRP
C3a and C4a
B12 and folic acid
Vitamin D: hydroxy 25 and didroxy 1,25
CD57- if covered by insurance
ANA
Rheumatoid factor
Bartonella antibody panel
RPR- HIV and hepatitis screen where appropriate
Babesia antibody panel: microti and WA1- although the name has been changed to duncani, Labcorp and Quest only know it by this name
Ehrilchia antibody panel plus Anaplasmosis
Lyme ELIZA C6 peptide index
Lyme Western Blot: 14IgM and 14 IgG bands- if the patient cannot afford the test I will first obtain the 13 blot test- I still get many positives
Wet mount examination of patient's blood
Only the expanded Lyme Western Blot and the Wet mount need to be performed by specialty labs
If further co-infection testing is required then Babesia species and Bartonella species by PCR may be obtained. A FISH test exists for Babesia- I have not generally ordered this test
Mycoplasm fermentans is a tick borne organism. It can only be demonstrated by PCR. An antibiotic active against Mycoplasm species should be given first to increase yield. Alternatively, a Mycoplasma species PCR may be ordered- this has a higher yield. It may demonstrate the presence of non-tick borne tissue organisms. I do not generally order this test
Another other non tick borne organism which I sometimes test for is Chlamydia pneumonia. This is an antibody test. PCR is also available- but is rarely positive
Fluids such as synovial fluid are tested for Lyme antibodies, C6 peptide index and Lyme PCR
Testing for viruses, such as EBV does not change my therapy- these tests only cause confusion- so I do not order them
Patients with fatigue- nearly everyone, gets a sleep study- sleep disorders are incredibly common in this group of patients
Patients with cognitve issues get brain MRI and SPECT scan
This is my basic set of tests for many patients
CBC
Chem panel-CMP
Sed rate
CRP
C3a and C4a
B12 and folic acid
Vitamin D: hydroxy 25 and didroxy 1,25
CD57- if covered by insurance
ANA
Rheumatoid factor
Bartonella antibody panel
RPR- HIV and hepatitis screen where appropriate
Babesia antibody panel: microti and WA1- although the name has been changed to duncani, Labcorp and Quest only know it by this name
Ehrilchia antibody panel plus Anaplasmosis
Lyme ELIZA C6 peptide index
Lyme Western Blot: 14IgM and 14 IgG bands- if the patient cannot afford the test I will first obtain the 13 blot test- I still get many positives
Wet mount examination of patient's blood
Only the expanded Lyme Western Blot and the Wet mount need to be performed by specialty labs
If further co-infection testing is required then Babesia species and Bartonella species by PCR may be obtained. A FISH test exists for Babesia- I have not generally ordered this test
Mycoplasm fermentans is a tick borne organism. It can only be demonstrated by PCR. An antibiotic active against Mycoplasm species should be given first to increase yield. Alternatively, a Mycoplasma species PCR may be ordered- this has a higher yield. It may demonstrate the presence of non-tick borne tissue organisms. I do not generally order this test
Another other non tick borne organism which I sometimes test for is Chlamydia pneumonia. This is an antibody test. PCR is also available- but is rarely positive
Fluids such as synovial fluid are tested for Lyme antibodies, C6 peptide index and Lyme PCR
Testing for viruses, such as EBV does not change my therapy- these tests only cause confusion- so I do not order them
Patients with fatigue- nearly everyone, gets a sleep study- sleep disorders are incredibly common in this group of patients
Patients with cognitve issues get brain MRI and SPECT scan
This is my basic set of tests for many patients
Localized Herx: knee
A patient presented to me with an acute swollen knee. She had been healthy until another physician prescribed a course of Cipro for a urinary tract infection.
She had typical mono-articular arthritis: arthritis of a single joint. The knee was swollen, red an hot with a large effusion. The patient tested positive for Lyme disease and was successfully treated.
This- I think may demonstrate the concept which I alluded to in the response to my last entry. First of all many ostensibly healthy persons are infected with sub-clinical Lyme. Something- many things, can set off the disease. Second, Herxes can be very localized, presenting in a specific area.
Many thinking in this case was that the Lyme organisms were present in the synovial tissues of this patent's knees. Cipro, a quinolone, was able to have exceptional penetration in to these tissues. As a result, this localized Herx occurred in the patient's knee. Post-quinolone treatment relied on less potent antibiotic, which have less penetration into synovial tissues. These tissues are minimally penetrated by most other antibiotics.Therapy with Amoxil and Biaxin, over time, was successful:swelling and arthritis gradually improved.
It is pure conjecture. I simply ask the question: could tendon rupture seen with quinolones represent a similar reaction?
She had typical mono-articular arthritis: arthritis of a single joint. The knee was swollen, red an hot with a large effusion. The patient tested positive for Lyme disease and was successfully treated.
This- I think may demonstrate the concept which I alluded to in the response to my last entry. First of all many ostensibly healthy persons are infected with sub-clinical Lyme. Something- many things, can set off the disease. Second, Herxes can be very localized, presenting in a specific area.
Many thinking in this case was that the Lyme organisms were present in the synovial tissues of this patent's knees. Cipro, a quinolone, was able to have exceptional penetration in to these tissues. As a result, this localized Herx occurred in the patient's knee. Post-quinolone treatment relied on less potent antibiotic, which have less penetration into synovial tissues. These tissues are minimally penetrated by most other antibiotics.Therapy with Amoxil and Biaxin, over time, was successful:swelling and arthritis gradually improved.
It is pure conjecture. I simply ask the question: could tendon rupture seen with quinolones represent a similar reaction?
Wednesday, June 10, 2009
Cipro for Lyme: Back to the future
A 60 year old female came to my office over one year ago. She had been struggling with fibromyalgia, ulcerative colitis and depression for decades. She provided a multi-page list of symptoms. The highlights were: fatigue, pain, loss of sensations, symptoms related to special senses--hearing-vision, AND rather profound cognitive deficits. She was on a list of nutritional supplements which filled a full page. She had been a highly functional professional in the past. She suspected she might have chronic Lyme disease; this diagnosis had never been made.
She brought sheaves of lab work which was unhelpful. I found her to have an elevated rheumatoid factor-(174)-normal less then 14. Her white blood cell count was minimally depressed, 3.7. Her CD57 was slightly depressed, 50. Special Clongen labs showed positive 39 and 23 Western Blot bands. A wet mount exam showed round extracellular bacteria.
The initial physical exam revealed a fairly profound peripheral neuropathy.
Her treatment was complex; she was prescribed a number of antibiotic combinations.
I will not discuss all the antibiotics she has taken over time, except to say that she was aggressively treated for the known co-infections.
One drug which has been particularly efficacious is Cipro. When this was discontinued she has back-pedaled everytime: symptoms which had improved return.
When I started treating chronic Lyme in a serious way, several years ago, I was sent a paper written by Dr. Jemsek. He described a Lyme regimen in which he used Cipro with Doxycyline. He stated that the two drugs worked via an intracellular mechanism and were synergistic.
After reading this I jumped on the Cipro train. Old data on MICs(minimal inhibitory concentrations), showed that Cipro was reasonably active against Bb.
I used Doxy and Cipro and then began switching to Cipro and Amoxicillin.
Doxycyline works by inhibiting protein synthesis within bacteria. Cipro works by inhibiting DNA gyrase necessary for DNA synthesis. Rather than using two intracellular antibiotics I combined a cell wall inhibitor with an intracellular antibiotic with the belief that this might be more effective. This sort of thinking was espoused by many LLMDS if not this particular combination.
In those days I wasn't giving Bartonella much thought, but it is well known that Cipro has activity against Bartonella.
I had years of experience with Cipro prior to launching into the the waters of Lyme. The tendon rupture issue is much exaggerated in my experience. What I know about Cipro is that it is a very powerful antibiotic. It has been claimed that oral Cipro can provide tissue antibiotic levels rivaling that of IV antibiotics. Cipro is one of the few antibiotics able to cross the prostate/blood barrier. Very high tissue concentrations--in many organs, are achieved with oral doses.
As I look back at charts of patients treated with Cipro I find that many had excellent responses. Then I stopped using Cipro for the most part: it was not an LLMD recommended drug.
As of late I am using the drug more. It provides high tissue concentrations, is active against Bb- and also works for Bartonella-or Bartonella syndrome.
I start low: 250 mg daily-- and then increase to 250mg twice daily. This relatively low dose is frequently effective. Patients are warned about tendon/muscle pain. I generally institute it when these pains have already been controlled by other antibiotics. I have never seen a tendon rupture.
As aside, Cipro is also active against Mycoplasmas and Chlamydia pneumonia.
It works.
She brought sheaves of lab work which was unhelpful. I found her to have an elevated rheumatoid factor-(174)-normal less then 14. Her white blood cell count was minimally depressed, 3.7. Her CD57 was slightly depressed, 50. Special Clongen labs showed positive 39 and 23 Western Blot bands. A wet mount exam showed round extracellular bacteria.
The initial physical exam revealed a fairly profound peripheral neuropathy.
Her treatment was complex; she was prescribed a number of antibiotic combinations.
I will not discuss all the antibiotics she has taken over time, except to say that she was aggressively treated for the known co-infections.
One drug which has been particularly efficacious is Cipro. When this was discontinued she has back-pedaled everytime: symptoms which had improved return.
When I started treating chronic Lyme in a serious way, several years ago, I was sent a paper written by Dr. Jemsek. He described a Lyme regimen in which he used Cipro with Doxycyline. He stated that the two drugs worked via an intracellular mechanism and were synergistic.
After reading this I jumped on the Cipro train. Old data on MICs(minimal inhibitory concentrations), showed that Cipro was reasonably active against Bb.
I used Doxy and Cipro and then began switching to Cipro and Amoxicillin.
Doxycyline works by inhibiting protein synthesis within bacteria. Cipro works by inhibiting DNA gyrase necessary for DNA synthesis. Rather than using two intracellular antibiotics I combined a cell wall inhibitor with an intracellular antibiotic with the belief that this might be more effective. This sort of thinking was espoused by many LLMDS if not this particular combination.
In those days I wasn't giving Bartonella much thought, but it is well known that Cipro has activity against Bartonella.
I had years of experience with Cipro prior to launching into the the waters of Lyme. The tendon rupture issue is much exaggerated in my experience. What I know about Cipro is that it is a very powerful antibiotic. It has been claimed that oral Cipro can provide tissue antibiotic levels rivaling that of IV antibiotics. Cipro is one of the few antibiotics able to cross the prostate/blood barrier. Very high tissue concentrations--in many organs, are achieved with oral doses.
As I look back at charts of patients treated with Cipro I find that many had excellent responses. Then I stopped using Cipro for the most part: it was not an LLMD recommended drug.
As of late I am using the drug more. It provides high tissue concentrations, is active against Bb- and also works for Bartonella-or Bartonella syndrome.
I start low: 250 mg daily-- and then increase to 250mg twice daily. This relatively low dose is frequently effective. Patients are warned about tendon/muscle pain. I generally institute it when these pains have already been controlled by other antibiotics. I have never seen a tendon rupture.
As aside, Cipro is also active against Mycoplasmas and Chlamydia pneumonia.
It works.
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